For research use only.
CAS No. 19774-82-4
Amiodarone HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias.
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Drugs across therapeutic indications induce lipid formation in hiPS-CM. Lipid accumulation was detected in cardiac cells using the LipidTox plate-based fluorescent assay on the Thermo Scientific CellInsight High Content platform. A) Ten drugs increased lipid levels in hiPS-CM following 48 h treatment. The lowest drug dose that induced a N1.5-fold increase in lipid formation is shown. B) Representative images (20×) from the assay are shown to the right. All drugs had >55% cell viability at 48 h at these tested concentrations. C) Of these 10 drugs, 8 significantly increased lipid accumulation following only 24 h treatment (images not shown). All drugs had >80% cell viability at 24 h at these drug doses. The graphs represent the mean fold-change of the lowest concentration of drug that significantly induced lipid formation >1.5-fold more than vehicle control. *P<0.05, **P<0.01, and ***P<0.0001.
Toxicol Appl Pharmacol, 2015, 285(1):51-60.. Amiodarone HCl purchased from Selleck.
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|Description||Amiodarone HCl is a sodium/potassium-ATPase inhibitor and an autophagy activator, used to treat various types of cardiac dysrhythmias.|
Amiodarone possesses an inhibitory effect on the fast sodium channel as well as on the slow calcium channel. Amiodarone also has non-competitive antisympathetic effects, and modulates thyroid function and phospholipid metabolism. Amiodarone penetrates deeply into the lipid matrix of the membrane, and is released from cardiac tissues very slowly when washed out. Amiodarone (44–88 μM) depresses Vmax of guinea pig papillary muscle without affecting the resting membrane potential, and that this Vmax inhibition is enhanced in a frequency- or use-dependent manner like Class I antiarrhythmic drugs. Amiodarone (50–88 μM) is also found to suppress the depolarization-induced spontaneous action potentials (abnormal automaticity) in ventricular muscles and in Purkinje fibers. 
|In vivo||Amiodarone (1.25–25 mg/kg) results in a decrease in sinus rate, a prolongation of effective and functional refractory periods of the atrioventricular node, and a frequency-dependent conduction delay in the atrioventricular node and in the ventricle of anesthetized dogs. Amiodarone (50 mg/kg/day, i.p. for 3–4 weeks) results in significant decreases in the current density of iK and ito in ventricular cells without affecting iCa and iK1 densities in rabbit. Amiodarone (AM) inhibits intracellular conversion from thyroxine (T4) to triiodothyronine (T3) via 5′-deiodination (5′DI) without affecting intracellular conversion from T4 to reverse T3 (rT3). |
|In vitro||DMSO||23 mg/mL (33.73 mM)|
|Ethanol||11 mg/mL (16.13 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
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Clinical Trial Information
|NCT Number||Recruitment||interventions||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03991754||Not yet recruiting||Procedure: transcatheter aortic valve implantation||Atrial Fibrillation New Onset||Luis Nombela Franco|Hospital San Carlos Madrid||June 30 2019||Phase 3|
|NCT03842020||Recruiting||Other: Blood pharmacokinetic samples||Heart Rhythm Disorder||Assistance Publique - Hôpitaux de Paris|URC-CIC Paris Descartes Necker Cochin||February 13 2019||Not Applicable|
|NCT03919097||Recruiting||Other: Medical Data extraction||Flutter||José Castro|Brugmann University Hospital||January 8 2019||--|
|NCT02783976||Completed||Drug: Sovaldi||HCV Infection||Gilead Sciences||October 28 2016||--|
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